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dc.contributor.author
Werz, Christian
dc.contributor.author
Köhler, Katja
dc.contributor.author
Hafen, Ernst
dc.contributor.author
Stocker, Hugo
dc.date.accessioned
2018-10-22T15:11:32Z
dc.date.available
2017-06-08T22:03:32Z
dc.date.available
2018-10-22T15:11:32Z
dc.date.issued
2009-08-14
dc.identifier.issn
1553-7390
dc.identifier.issn
1553-7404
dc.identifier.other
10.1371/journal.pgen.1000596
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/16303
dc.identifier.doi
10.3929/ethz-b-000016303
dc.description.abstract
Insulin/insulin-like growth factor signaling (IIS) plays a pivotal role in the regulation of growth at the cellular and the organismal level during animal development. Flies with impaired IIS are developmentally delayed and small due to fewer and smaller cells. In the search for new growth-promoting genes, we identified mutations in the gene encoding Lnk, the single fly member of the SH2B family of adaptor molecules. Flies lacking lnk function are viable but severely reduced in size. Furthermore, lnk mutants display phenotypes reminiscent of reduced IIS, such as developmental delay, female sterility, and accumulation of lipids. Genetic epistasis analysis places lnk downstream of the insulin receptor (InR) and upstream of phosphoinositide 3-kinase (PI3K) in the IIS cascade, at the same level as chico (encoding the single fly insulin receptor substrate [IRS] homolog). Both chico and lnk mutant larvae display a similar reduction in IIS activity as judged by the localization of a PIP3 reporter and the phosphorylation of protein kinase B (PKB). Furthermore, chico; lnk double mutants are synthetically lethal, suggesting that Chico and Lnk fulfill independent but partially redundant functions in the activation of PI3K upon InR stimulation.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Public Library of Science (PLoS)
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.title
The Drosophila SH2B family adaptor Lnk acts in parallel to chico in the insulin signaling pathway
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
ethz.journal.title
PLoS Genetics
ethz.journal.volume
5
en_US
ethz.journal.issue
8
en_US
ethz.journal.abbreviated
PLoS Genet
ethz.pages.start
e1000596
en_US
ethz.size
9 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.nebis
005410305
ethz.publication.place
San Francisco, CA
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2017-06-08T22:03:38Z
ethz.source
ECIT
ethz.identifier.importid
imp59364c627fa6993683
ethz.ecitpid
pub:28168
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-12T11:04:31Z
ethz.rosetta.lastUpdated
2018-10-22T15:11:37Z
ethz.rosetta.versionExported
true
ethz.COinS
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